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s discussed in my recent book, The Top 10 Lyme Disease Treatments, there is currently a heated debate surrounding the question of whether the chronic form of Lyme Disease is a real medical condition caused by Lyme Disease bacteria, or instead, a psychosomatic condition caused by paranoia or other mental factors. 

The Infectious Disease Society of America (IDSA), which is generally recognized as the authority on topics relating to infectious diseases (including Lyme Disease), does not recognize that chronic Lyme Disease is caused by an active bacterial infection. On the other side of the debate reside thousands of Lyme Disease patients and physicians who believe that chronic Lyme Disease is in fact caused by the persistent presence of an active infection. 

IDSA guidelines generally determine Centers for Disease Control (CDC) guidelines, and CDC guidelines generally determine what is and is not accepted practice for licensed physicians. Hence, because the IDSA does not recognize chronic Lyme Disease as a real medical condition, neither do the majority of physicians in the United States.

Before moving on, let’s clarify what the debate is actually about. The IDSA does not deny the existence of Lyme Disease itself—the

 organization recognizes Lyme Disease as a significant bacterial infection. What the IDSA disagrees with is the position that active Lyme Disease bacteria can persist inside the human body after a standard course of antibiotics is administered. IDSA acknowledges Lyme Disease, and understands that it is dangerous, but the organization takes the stance that the disease always goes away after it is treated with a few weeks of antibiotics. The IDSA does recognize a syndrome in which people who have suffered from Lyme Disease experience ongoing symptoms after antibiotic therapy. However, according to the IDSA, this syndrome (which they refer to as "post-Lyme syndrome") is not caused by infection with Lyme Disease bacteria, but instead, psychosomatic factors such as hypochondria and laziness.

For people suffering with chronic Lyme Disease, IDSA guidelines can be devastating. Yes, the IDSA does recognize "post-Lyme syndrome," but only as a psychosomatic disorder—not as an active bacterial infection. Why does it matter whether or not the IDSA believes chronic Lyme Disease is caused by active bacteria or paranoia? Actually, it matters a lot. Although the IDSA does recognize post-Lyme syndrome, their stance on the cause of the disease makes the difference between Lyme Disease sufferers being vindicated and receiving the treatment they need, or being ridiculed and denied appropriate treatment. Current IDSA guidelines stipulate that doctors should treat chronic Lyme Disease with psychological counseling, and if that does not work, doctors should simply throw patients out of the office and tell them they are crazy. When doctors attempt to treat a raging bacterial infection as if it were paranoia or a character flaw, the result is a large number of very sick patients being talked at instead of disinfected. Additionally, treating chronic Lyme Disease as a psychological problem also results in the ridiculing and disparaging of Lyme patients when the therapy doesn't work and symptoms persist. 

On the other hand, if chronic Lyme Disease is treated appropriately with antibacterial therapies, patients will actually get better, get support in areas that matter (emotional, insurance coverage, and understanding from employers and family members), and get compassion during ongoing sickness. So, as you can see, the question of the cause of chronic Lyme Disease is of critical importance to those suffering from the condition.

In recent months the debate has only become more intense, and its resolution seems as far off as ever. On October 4, 2007, the New England Journal of Medicine (one of the most well-respected and credible medical organizations in the world) published an article entitled A Critical Appraisal of “Chronic Lyme Disease,” authored by Henry M. Feder, Jr., M.D., Barbara J.B. Johnson, Ph.D., Susan O'Connell, M.D., Eugene D. Shapiro, M.D., Allen C. Steere, M.D., Gary P. Wormser, M.D., and the Ad Hoc International Lyme Disease Group. 

The report begins with accurate information: 

“Lyme Disease, the most common tick-borne infection in the northern hemisphere, is a serious public health problem. In North America, it is caused exclusively by Borrelia burgdorferi sensu stricto (hereafter referred to as B. burgdorferi), whereas in Europe it is caused by B. afzelii, B. garinii, B. burgdorferi, and occasionally by other species of Borrelia.”

However, after this statement, not much else in the report bears resemblance to reality. The authors recognize that “…after antibiotic treatment, a minority of patients have fatigue, musculoskeletal pain, difficulties with concentration or short-term memory, or all of these symptoms.” But, instead of attributing these symptoms to an active bacterial infection, the article states that “Data from controlled trials have shown that there is substantial risk, with little or no benefit, associated with additional antibiotic treatment for patients who have long-standing subjective symptoms after appropriate initial treatment for an episode of Lyme Disease.” Furthermore, the article dismisses the improvements attained by patients who have received benefit from long-term antibiotic treatment: “Although anecdotal evidence and findings from uncontrolled studies have been used to provide support for long-term treatment of chronic Lyme Disease, a response to treatment alone is neither a reliable indicator that the diagnosis is accurate nor proof of an antimicrobial effect of treatment.” 

Finally, the article concludes by stating that “It is highly unlikely that post–Lyme Disease syndrome is a consequence of occult infection of the central nervous system.” The following advice is offered to clinicians who see patients claiming to have chronic Lyme Disease:

“How should clinicians handle the referral of symptomatic patients who are purported to have chronic Lyme Disease? The scientific evidence against the concept of chronic Lyme Disease should be discussed and the patient should be advised about the risks of unnecessary antibiotic therapy. The patient should be thoroughly evaluated for medical conditions that could explain the symptoms. If a diagnosis for which there is a specific treatment cannot be made, the goal should be to provide emotional support and management of pain, fatigue, or other symptoms as required. Explaining that there is no medication, such as an antibiotic, to cure the condition is one of the most difficult aspects of caring for such patients. Nevertheless, failure to do so in clear and empathetic language leaves the patient susceptible to those who would offer unproven and potentially dangerous therapies.”

It is not difficult to imagine the damaging and completely counterproductive effects this article will have on sufferers of chronic Lyme Disease. This new report raises the stakes considerably and renders an already red-hot, hostile environment, even more perilous. The suffering and despair of the Lyme Disease community appears to be headed for a turn for the worse, if that is even possible given the current state of abandon and disparagement it is already experiencing.

The Hartford Courant, on October 5, 2007, reports the response of Dr. Raphael Stricker, president of the International Lyme Disease Association (ILADS), to the article: “It's a disaster for people with chronic Lyme Disease…since it appeared in the New England Journal of Medicine, everyone will take it as dogma and nobody [referring to insurance companies] will want to pay for treatment.''

Pat Smith, president of the Lyme Disease Association (LDA) had a similar response to the New England Journal of Medicine article: "It is just the same old people saying the same old thing. They just choose to select one set of research and ignore other research.''

This chapter will examine what the scientific literature actually says, in an attempt to reveal the truth. The New England Journal of Medicine article claims that “Chronic Lyme Disease is the latest in a series of syndromes that have been postulated in an attempt to attribute medically unexplained symptoms to particular infections. Chronic Lyme Disease is a misnomer, and the use of prolonged, dangerous, and expensive antibiotic treatments for it is not warranted.” Is this a true statement? You decide after reviewing the evidence. The studies we will look at below have been conducted all over the world and represent an objective and diverse cross-section of modern Lyme Disease research. Please keep in mind that the following collection of scientific studies represents only a small sampling of the available, relevant articles—there are many more research summaries available than space in this book will permit.

The science is clear

Let's start by examining the findings of the Institute of Rheumatology, in Prague, Czech Republic. Physicians in Prague report a case of a female patient suffering from Lyme Disease. Her case was confirmed by detection of Borrelia garinii DNA present in her blood and synovial fluid. After treatment with antibiotics, symptoms persisted and six months later, Borrelia garinii DNA was "repeatedly detected in the synovial fluid and the tissue of the patient." Additionally, even after antibiotic therapy, antigens and parts of spirochetes were detected by electron microscopy in the synovial fluid, tissue, and blood. 

A similar discovery was made in Germany at the University Hospital of Frankfurt. Researchers describe Lyme Disease as a "disorder of potentially chronic proportions." They also note that "therapeutic failures have been reported for almost every suitable antimicrobial agent currently available and resistance to treatment...continues to pose problems for clinicians in the management of patients suffering from chronic Lyme Disease." Another University in Germany, Ludwig-Maximilians-University, located in Munich, reported that "failures in the antibiotic therapy of Lyme Disease have repeatedly been demonstrated by post-treatment isolations of the infecting Borreliae." 

One of the most interesting German studies, completed at Ludwig-Maximilians-Universitat Munich, attributed the clinical persistence of Lyme Disease after antibiotic therapy to the presence of variants and atypical forms of B. burgdorferi. In fact, similar to the conclusion I draw in my book Lyme Disease and Rife Machines, German researchers conclude that "B. burgdorferi produce spheroplast- L-form variants...these forms without cell walls can be a possible reason why Borrelia survive in the organism for a long time (probably with all beta-lactam antibiotics) and the cell wall-dependent antibody titers disappear and emerge after reversion." 

Researchers at the University of Dermatologische Privatpraxis, Munich, Germany, agree with their German peers in a 1996 study which notes that patients with erythema migrans can fail to respond to antibiotic therapy. “Persistent or recurrent erythema migrans, major sequelae such as meningitis and arthritis, survival of Borrelia burgdorferi and significant and persistent increase of antibody titres against B. burgdorferi after antibiotic therapy are strong indications of a treatment failure. Most, if not all, antibiotics used so far have been associated with a treatment failure in patients with erythema migrans.” 

In Austria, in 2001, the Lainz Municipal Hospital in Vienna admitted a 64 year-old woman who presented with various systemic symptoms hinting of Lyme Disease. Spirochetes were detected in samples of her skin lesions. Shortly thereafter, a diagnosis of Lyme Disease was made. According to doctors, "despite treatment with four courses of intravenous ceftriaxone for up to 20 days, progression of [Lyme symptoms] was only stopped for a maximum of one year.” A nearby hospital in Graz, Austria, studied four cases of verified late stage Lyme Disease and found that serology was Lyme-positive even after repeated courses of high-dose intravenous penicillin-G and/or cephalosporins.

Researchers at the Turku University Central Hospital, Finland, conducted a study in which 165 patients with disseminated Lyme Disease were followed after antibiotic treatment. Approximately 10% of the patients experienced a clinical relapse with positive PCR tests and spirochetes successfully cultured from the blood of the patients. Note, in this case, that the Lyme Disease relapse was not evidenced only by continuing symptoms, but also by two independent testing methods: both PCR testing and blood culture. This single study, even without aid from the numerous other studies presented in this chapter, should be enough to call into question the IDSA's staunch and dogmatic stance on chronic Lyme Disease. 

Italy also has experience with chronic Lyme Disease. In 1992, the Universita di Genova, located in Genoa, Italy, reported on two patients with "chronic Lyme arthritis resistant to the recommended antibiotic regimens." These patients were eventually cured by long term treatment with benzathine penicillin. The Italian researchers who conducted this study offered two possible reasons why antibiotic therapy finally worked, and both of these reasons involve active, persistent infection: "the sustained therapeutic levels of penicillin were effective either by the inhibition of germ replication or by lysis of the spirochaetes when they were leaving their sanctuaries." 

Moving across the globe to Thailand, scientists at KhonKaen University write that "Electron microscopy adds further evidence for persistence of spirochetal antigens in the joint in chronic Lyme Disease. Locations of spirochetes or spirochetal antigens both intracellulary and extracellulary in deep synovial connective tissue as reported here suggest sites at which spirochetes may elude host immune response and antibiotic treatment."

In France, a study was published in the Journal of Antimicrobial Agents and Chemotherapy in 1996, conducted by the University of Marseille. The study notes that "despite appropriate antibiotic treatment, Lyme Disease patients may have relapses or may develop chronic manifestations."

It would be understandable for the IDSA to neglect, or at least take less seriously, research conducted outside the borders of the United States, since the IDSA is an organization that operates inside, and is accountable to, U.S. citizens and the U.S. government. However, as we move in to examine studies conducted in the United States, you will see that a significant portion of the evidence in favor of chronic Lyme Disease actually originated here on American soil.

In 1996, the Fox Chase Cancer Center in Philadelphia, Pennsylvania, conducted a study in which it was discovered that urine samples from 97 patients clinically diagnosed with chronic Lyme Disease contained Borrelia Burgdorferi DNA. The interesting aspect of this finding is that most of these patients had previously been treated with extended courses of antibiotics, the implications of which are simply that antibiotic therapy (even extended courses) does not always eradicate the infection. The study concludes that "a sizeable group of patients diagnosed on clinical grounds as having chronic Lyme Disease may still excrete Borrelia DNA, and may do so in spite of intensive antibiotic treatment."

The State University of New York at Stony Brook conducted a study in 1996 to determine which of two types of antibiotic (azithromycin or amoxicillin) is more efficacious for the treatment of early Lyme Disease. The study found that amoxicillin was more effective than azithromycin. However, more interestingly, patients from each group did experience relapses despite antibiotic therapy. 

While the IDSA was releasing their guidelines in which it was concluded that chronic Lyme Disease is not a medical condition that justifies extended antibiotic therapy, researchers at the New York State Psychiatric Institute were discovering just the opposite. The authors of a report produced at that institution describe a case of fatal neuropsychiatric Lyme Disease that was "expressed clinically by progressive frontal lobe dementia and pathologically by severe subcortical degeneration." When describing the situation, doctors note that "antibiotic treatment resulted in transient improvement, but the patient relapsed after the antibiotics were discontinued...prolonged antibiotic therapy may be necessary [in some cases]."

In Boston, Massachusetts, researchers at Tufts University School of Medicine encountered similar findings when investigating Borrelia's ability to attach to and invade human fibroblasts in vitro. "By scanning electron microscopy, B. burgdorferi were tightly adherent to fibroblast monolayers after 24-48 hours but were eliminated from the cell surface by treatment with ceftriaxone (1 microgram/mL) for 5 days. Despite the absence of visible spirochetes on the cell surface after antibiotic treatment, viable B. burgdorferi were isolated from lysates of the fibroblast monolayers. B. burgdorferi were observed in the perinuclear region within human fibroblasts by laser scanning confocal microscopy. Intracellular spirochetes...were also identified by fluorescent laser scanning confocal microscopy. These observations suggest that B. burgdorferi can adhere to, penetrate, and invade human fibroblasts in organisms that remain viable.”

In a separate report, Tufts University researchers conducted a study to investigate neurologic abnormalities found in chronic Lyme Disease sufferers; 27 patients were followed. Six months after a two-week course of intravenous ceftriaxone (2 g daily), 17 patients showed improvement, 6 had improvement but then relapsed, and 4 had no change in their condition. Researchers conclude that "months to years after the initial infection with B. burgdorferi, patients with Lyme Disease may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis." With regard to the cause of chronic Lyme Disease, Tufts University implies a bacterial origin with their closing statement in the study: "These chronic neurologic abnormalities usually improve with antibiotic therapy."

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In 1992, Tufts University presented a hypothesis which might explain how Lyme Disease bacteria become resistant to antibiotics and host immune response. Researchers note that "since B. burgdorferi first infects skin, the possible protective effect of skin fibroblasts from antibiotics was examined. We found that human foreskin fibroblasts protected B. burgdorferi from the lethal action of a 2-day exposure to ceftriaxone." The researchers conclude that "the Lyme Disease spirochete, Borrelia burgdorferi, can be recovered long after initial infection, even from antibiotic-treated patients, indicating that it resists eradication by host defense mechanisms and antibiotics."

At Thomas Jefferson University, Philadelphia, Pennsylvania, urologists who treated seven patients with Lyme Disease found that "neurological and urological symptoms in all patients were slow to resolve and convalescence was protracted...relapses of active Lyme Disease and residual neurological deficits were common." 

In direct opposition to IDSA statements, researchers at the Department of Pathology, Southampton Hospital, New York, note that active cases of Lyme Disease may show clinical relapse following antibiotic therapy. It is noted that "the latency and relapse phenomena suggest that the Lyme Disease spirochete is capable of survival in the host for prolonged periods of time." In their studies of 63 patients with Lyme Disease, the researchers conclude that "some patients with Lyme Borreliosis may require more than the currently recommended two to three week course of antibiotic therapy..."

Also in the State of New York, the New York University School of Medicine conducted a study which evaluated antibiotic treatment of 215 patients between the years 1981 and 1987. Of those with "major" Lyme Disease manifestations, a relapse rate of over 20% was observed. 

This next study is interesting for several reasons, as we will see. The Albert Einstein College of Medicine, New York, reported in 1995 an "unusual" case of Lyme Disease in which the patient experienced repeated neurologic relapses despite aggressive antibiotic therapy. What makes this study interesting is that each subsequent course of antibiotics given after the relapses was followed by Jarisch-Herxheimer reactions, which are known to occur only when active bacteria are dying, which implies that active bacteria were still present in the body after multiple courses of antibiotics. Additionally, subsequent to the various courses of antibiotics, the patient’s cerebral spinal fluid tested positive "on multiple occasions" for not only complex anti-Borrelia antibodies, but also Borrelia nucleic acids and free antigen proteins. This study demonstrates persistent infection via two separate indicators: repeated Jarisch-Herxheimer reactions, and repeated observation of antibodies and antigens. Both indicators were found after not just one, but multiple courses of "adequate antibiotic therapy" had been administered!

One of the peculiar aspects of the above study is that the patient was referred to as "unusual.” Is this an accurate characterization? Are such incidences really unusual? Actually, they are quite common. In Aurora, Colorado, at the Fitzsimons Army Medical Center, a patient presented with chronic septic Lyme arthritis of the knee. This patient had experienced symptoms for seven years despite "multiple antibiotic trials and multiple arthroscopic and open synovectomies." Polymerase chain reaction (PCR) analysis of the tissue was consistent with Borrelia infection, so a diagnosis of Lyme Disease followed. The most interesting part of this study is that, after the diagnosis of Lyme Disease was made, and after multiple courses of antibiotics were administered, spirochetes were documented in synovium and synovial fluid. 

Another similar case observed in Bethesda, Maryland, further calls into question the statement that chronic, persistent Lyme Disease infection is "unusual." Doctors in Maryland working with the National Institute of Arthritis and Musculoskeletal and Skin Diseases, a part of the National Institutes of Health (NIH), report a 40-year-old white man who developed clinical Lyme Disease after being bitten by a tick. He was treated with oral tetracycline, after which his symptoms were resolved. However, at a later date, the man was re-tested and Borrelia was detected by PCR in his peripheral blood leukocytes. After being re-treated with a longer course of ampicillin, probenicid, and concurrent cytotoxic therapy, symptoms improved significantly. This individual's case of Lyme Disease illustrates two important points: First, ongoing symptoms after antibiotic therapy were confirmed by PCR testing to be caused by active bacteria. Second, re-treatment with antibiotics resulted in significant clinical improvement.

Turning our attention back to New York, let’s look at a study conducted on animals at the Baker Institute for Animal Health at Cornell University in Ithaca. Antibiotic treatment of Lyme-infected dogs was studied over the course of 30 days. The study concludes that "B. burgdorferi disseminates through tissue by migration following tick inoculation, produces episodes of acute arthritis, and establishes persistent infection...the spirochete survives antibiotic treatment and disease can be reactivated." 

The Baker Institute for Animal Health conducted a second, similar study which drives the point home even more clearly. This time, researchers experimentally infected healthy dogs via tick bites with Borrelia burgdorferi. The infected dogs were then treated for 30 days with high doses of amoxicillin or doxycycline. Interestingly, although symptoms declined significantly after treatment, skin punch biopsies and multiple tissues from necropsy samples remained PCR positive. Moreover, and in direct support of the presence of an actual, persistent bacterial infection, Borrelia organisms were found in post-therapy dogs. Some dogs that were treated with antibiotics were kept in isolation for six months post-treatment. In most of these dogs, after six months, Lyme antibody levels began to increase again, "presumably in response to proliferation of the surviving pool of spirochetes." 

It is clear that Lyme Disease can persist inside the human body chronically. But how? I suggest reading my first book, Lyme Disease and Rife Machines, to read a thorough and fascinating account of what I refer to as the "Lyme Disease Defense Mechanism," which is the survival process that facilitates the persistence of Lyme Disease bacteria in almost any environment. In addition to the information found in that book, here is one new method of persistence which was just recently discovered: In a recent article published in The Journal of Microbes and Infection, researchers discovered the presence of "persister cells" in chronic infections, particularly Lyme Disease. These cells facilitate numerous means of bacterial resistance, including modification of host immune cells and enzymes, expulsion of antibiotics from cellular structures, restricted permeability to antibiotics, and creation of protective biofilms. The studies discussed in Lyme Disease and Rife Machines highlight the many additional strategies Lyme Disease bacteria employ to persist and survive despite immunological, therapeutic, and environmental challenges. 

What is the truth?

What does the literature tell us? If you take the time to read it and think about its implications, you'll find that the existence of chronic Lyme Disease (as caused by an active bacterial infection) is quite obvious and established. Numerous scientific studies, conducted across the globe by interdisciplinary scientists, have plainly shown this to be the case. The controversy is one of political and dogmatic origin, not of scientific origin. The IDSA denies an active bacterial infection as the cause of chronic Lyme Disease not as a result of scientific observation, but instead, because of various inefficiencies and shortcomings inherent in the bureaucratic procedures through which the IDSA operates. The process by which bureaucratic entities accept new truths, and grow in knowledge, has always been painfully slow and inefficient—and such is the case with the IDSA. Because chronic Lyme Disease is in fact real, I am confident that it will be recognized as such sooner or later. Unfortunately, in the meantime, patients are left to dangle in the gap between two sides of an academic debate.

After reading the above scientific literature, one cannot help but wonder why the New England Journal of Medicine would publish a statement such as this one, found in the October 4, 2007, article mentioned above:

“The lack of convincing evidence for the persistence of B. burgdorferi in treated patients is not surprising. The failure of treatment for bacterial infections typically occurs as a result of pathogens that either have or acquire resistance to antibiotics, difficulties in achieving sufficient concentrations of antibiotic at sites of infection, or impaired host-defense mechanisms. None of these factors are generally applicable to infection with B. burgdorferi. Although B. burgdorferi can develop into cyst-like forms in vitro under certain conditions that can be created in the laboratory, there is no evidence that this phenomenon has any clinical relevance. B. burgdorferi may penetrate cells in vitro, but there is no evidence that the organism may be sheltered from antibiotics during an intracellular phase and then disseminate and cause clinical relapse.”

Where are they getting this research? Is there a hidden set of scientific literature somewhere that only these authors have access to? How can the article make such sweeping, inaccurate claims? Any rational person would have to wonder, after reading the research, what forces motivate those who write such statements. It seems clear that whatever their motivation, it is not the presentation objective, scientific truth. This is frightening considering that these statements were published in a journal as prestigious and important as the New England Journal of Medicine. Medical truth is unfortunately not easy to find, even in the places you would expect most to see it.

In the year 2008, the number of organizations and researchers who do not acknowledge the chronic form of Lyme Disease can be counted on one hand. You want credible evidence? How about the Yale University School of Medicine. In a report published by Yale in September of 2004, researchers describe a newly-discovered “protective niche for Borrelia burgdorferi” that allows the infection to “evade immunity” leading to “chronic infection.” You can add Yale to the list of institutions that acknowledge Lyme Disease in its persistent, chronic form.

It is of critical importance that scientists, researchers, and doctors take steps to quickly correct erroneous conclusions about chronic Lyme Disease. It is literally a question of life or death. Right now, as you read this, there are thousands of desperate, debilitated, infected people being told that there is nothing wrong with them. Even in the year 2008, as modern medicine continues to provide solutions to so many health problems, there is a contingent of the population whose needs are being completely ignored. This is not acceptable and change must occur soon. Very soon. 

It seems appropriate to close this chapter, and, indeed, close this book, with a letter written by a New York physician who states the facts more articulately than I can. This letter—written by Dr. Richard Brand, M.D.—clearly sums up the current state of affairs. I leave you now with Dr. Brand’s words:

October 27, 2007

I have been trying to divine a reason why the various medical specialty organizations (Infectious Disease, Neurology and now, Dermatology) have been racing to perpetrate a preponderance of guidelines that denounce appropriate, or at least reasonable, diagnosis and treatment for one particular medical condition. I am aware of no parallel in any other illness. It is worthwhile to state that the surprising orgasm of guidelines follows no new research findings to account for the timing of their release. 

The reason for issuing guidelines was ostensibly to avert the danger of long term antibiotic treatment. I found this particularly confounding with regard to Dermatologists, who prescribe minocycline for years on end to treat, or sometimes prevent, acne, a far less debilitating condition than chronic Lyme disease. Also, recently humorously stated, long term antibiotic treatment has resulted in some of the healthiest cows and chickens the world has ever seen. 

Logically, either the NEJM physicians are all absolutely correct and the entire Lyme community is as misguided as they attest, and our doctors as mischievous or malevolent as they allege, or they themselves are either grossly mistaken or have some motive for their savage attacks on fellow physicians, and by extension, a large and growing population of suffering patients. 

Since they are not fools and they have access to the same database that we do, including their own previous studies attesting to the persistence of Lyme following treatment, they must have some motive. At first, I examined the disclosures and recognized some conflict of interest that might offer a rationale for a few in the NEJM group, but that did not account for the other professional groups joining in the fray, all in such a well timed and coordinated fashion. 

This afternoon, I discussed these events with a colleague (my wife, Jane Kelman, M.D.). If we are correct that Lyme has been misdiagnosed and under treated, and disability created wholesale through this negligence, and this becomes an accepted public reality, that is, the reality that we already know to be true, the inevitable medical malpractice suits will destroy those physicians responsible, represented by the three major medical specialties who have been the first contact for most patients with Lyme disease. Those are the very specialties now circling the wagons in a pre-emptive attack to preserve what they recognize is a massive, catastrophic error in analysis and judgment. 

While there may have been other, early motivations (the profit from vaccine development, legal testimony fees and so on), there is now one single, unifying, global reason to refute chronic Lyme: To protect themselves from the repercussions that will follow if, or rather when, the preponderance of Lyme cases and disseminated Lyme information reaches critical mass. They will try to argue standard of care by hiding behind their own guidelines and those of their closely related co-specialists. While they have different specialties, they have one common motive. This is defensive and possibly illegal manipulation of the first degree and it is the only explanation that makes sense of the whole. 

The current mania to produce guidelines has been driven by the recent explosion in Lyme information hitting every news media, with the recent publicity slanted invariably toward mentioning a controversy rather than merely stating the anti-Lyme position, as had been the case until recently. Major TV stations are picking up on the story, and now, with the Connecticut attorney general adding credibility, and President Bush’s treatment adding visibility, the anti-Lyme docs are in an understandable panic. This is beginning to look like their perfect storm, not ours. 

The attorney general of Connecticut is at least half right. He is focused on the antitrust implications, but, if he is not already, will become aware of the motive behind their conspiracy: Besides restraint of trade, the effect on many infectious disease, neurological and dermatological physicians will be massive lawsuits for negligence involving failure to properly diagnose and treat, with readily provable losses of health and income directly attributable to medical malpractice. 

I am elated by recent events. If the anti-Lyme doctors had simply muddled along, permitting a situation where some Lyme patients got treatment, some didn’t, and things were confused, they might have survived longer. However, probably a result of overactive egos, maybe the new preeminence of certain individuals, they decided to go in for the kill, staging the current guideline ploy to finish us off once and for all, literally killing us off by providing permission for insurance companies to deny treatment. This move, paradoxically, will prove to be their undoing, not ours, as it provides a prima facie case for conspiracy. 

We have only to keep telling the truth: That Dr. Feder et al make their case by selectively employing particular studies, avoiding others which refute their position, even ignoring their own past studies and pronouncements. Their duplicity is transparent and the heat is building. 

Richard Brand, M.D. 
120 N. Main St 
New City, NY 10956 

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